Key result
The presence of Chlamydia pneumoniae in carotid plaques was not associated with an increased risk of mortality, restenosis, or progression of carotid disease following endarterectomy (p>0.05).
Why the study?
Does the presence of Chlamydia pneumoniae in carotid plaques increase the risk of restenosis, progression, or mortality in patients following carotid endarterectomy?
Cohort (n=70)
Single-blind
No
Does the presence of Chlamydia pneumoniae in carotid plaques increase the risk of restenosis, progression, or mortality in patients following carotid endarterectomy?
p-value: p=>0.05
The presence of Chlamydia pneumoniae in carotid plaques does not appear to influence the risk of restenosis, disease progression, or mortality after carotid endarterectomy.
Chlamydia pneumoniae in plaques was not linked to worse post-CEA outcomes; leaves open its role in carotid atherosclerosis.
BACKGROUND: Seroepidemiological studies have shown an association between raised antibody titres against Chlamydia pneumoniae, and carotid atherosclerosis or stroke. However, direct evidence for a causal link between arterial infection with C. pneumoniae and carotid disease remains weak. We hypothesized that long-term follow-up of patients with pathologically-proven arterial C. pneumoniae infection might provide further insight into the role of C. pneumoniae in carotid atherosclerosis. METHODS: We followed a cohort of 70 carotid endarterectomy patients for ipsilateral restenosis, contralateral progression, and all-cause mortality (four year median follow-up period). All patients had presence or absence of C. pneumoniae in their carotid plaques documented by immunohistochemistry after endarterectomy. A survival function was generated and the log-rank test was used to assess the difference in survival between subjects with and without documented chlamydial infection in their plaque. RESULTS: Baseline demographic and cardiovascular risk factors were similar between the two groups, and survival analysis demonstrated no difference (p>0.05) in all-cause mortality, or all-cause mortality combined with restenosis and progression. CONCLUSIONS: Our data finds no causal role for C. pneumoniae in restenosis or progression of carotid disease or mortality in this patient population with advanced carotid atherosclerosis.
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Jahromi et al. (2003) conducted a cohort in Carotid atherosclerosis (n=70). Presence of Chlamydia pneumoniae in carotid plaques vs. Absence of Chlamydia pneumoniae in carotid plaques was evaluated on Combined outcome of all-cause mortality, ipsilateral restenosis, and contralateral progression (p=>0.05). The presence of Chlamydia pneumoniae in carotid plaques was not associated with an increased risk of mortality, restenosis, or progression of carotid disease following endarterectomy (p>0.05).
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